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Posted at the Institutional Resources for Unique Collection and Academic Archives at Tokyo Dental College, Available from http://ir.tdc.ac.jp/

Author(s)

Alternative Terakawa, Y; Ichinohe, T; Kaneko, Y

Journal Regional anesthesia and pain medicine, 34(6): 553-556

URL http://hdl.handle.net/10130/2185

Right

This is a non-final version of an article published in final form in Reg Anesth Pain Med. 2009 Nov-Dec;34(6):553-6

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Title Page

Redistribution of tissue blood flow after stellate ganglion block in the rabbit

Yui Terakawa, DDS* Tatsuya Ichinohe, DDS, PhD† Yuzuru Kaneko, DDS, PhD ‡

*Postgraduate student

†Professor and Chairman ‡Professor

Department of Dental Anesthesiology, Tokyo Dental College

Address correspondence to; Yui Terakawa, DDS

Department of Dental Anesthesiology, Tokyo Dental College

1-2-2, Masago, Mihama-ku, Chiba 261-8502, Japan

Telephone number: +81-43-270-3970

Fax number: +81-43-270-3971

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Financial source: n.a

Meetings: The 283th Annual meeting of Tokyo Dental College Society

The 36th Annual meeting of Japanese Dental Society of Anesthesiology

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Abstract

Background and Objectives: The goal of this study was to compare tissue blood flow at

various sites before and after stellate ganglion block (SGB), and discuss the redistribution of

tissue blood flow after SGB.

Methods: We utilized 16 male Japan White rabbits. For SGB, the tip of the 26-gauge needle

was placed on the left transverse process of the cervical vertebra, 1-2 mm caudal to the cricoid

cartilage. Either 0.2 ml of 1 % lidocaine (Lidocaine group) or normal saline solution (Saline

group) was injected. In Lidocaine group, data were recorded immediately before SGB and at

the time when the maximal change in common carotid artery blood flow (CCBF) was observed

after SGB. In Saline group, data were recorded immediately before SGB and 3 minutes after

SGB. Observed variables were blood pressure, heart rate, CCBF, tongue mucosal blood flow

(TMBF), mandibular bone marrow blood flow (BBF), masseter muscle blood flow (MBF),

quadriceps muscle blood flow (QBF), liver blood flow (LBF) and renal blood flow (RBF).

Results: CCBF, TMBF, BBF and MBF on the block side were increased whereas BBF and

MBF on the non-block side, QBF, LBF and RBF were decreased after SGB in Lidocaine

group.

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flow on the non-block side are redistributed to the block side after SGB. In addition,

redistribution from peripheral tissue may have more important role than that of visceral blood

flow after SGB.

Key Words: Stellate ganglion block - Redistribution of tissue blood flow - Face - Lower limb

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Introduction

Stellate ganglion block (SGB) increases regional tissue blood flow in head, face, neck and

upper limb depending on its sympatholytic effects.1 SGB is useful for the treatment of several

disorders such as orofacial pain including postherpetic neuralgia. 2,3

It has been reported that an increase in regional tissue blood flow on the block side is

attributable to the redistribution of that on the non-block side.4,5 Cerebral blood flow,4 and

common carotid arterial blood flow (CCBF) and brachial arterial and venous blood flow5 were

increased after SGB whereas those on the non-block side were decreased.4,5 Meanwhile, there

is a report that facial skin blood flow was bilaterally increased after SGB.6 In addition, blood

flow of celiac artery, which is not innervated by the cervical sympathetic fibers, was increased

after SGB.7 It is assumed that there should be a region where tissue blood flow decreases to

balance with increased blood flow on the block side after SGB because circulating blood

volume is constant. This blood flow decrease might result in inadequate tissue oxygenation at

these sites. However, the change of tissue blood flow distribution before and after SGB

remains unknown.

In this study, therefore, we compared tissue blood flow before and after SGB, and

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tongue mucosal blood flow (TMBF), mandibular bone marrow blood flow (BBF), masseter

muscle blood flow (MBF), quadriceps muscle blood flow (QBF), liver blood flow (LBF) and

(8)

Methods

Sixteen male Japan White rabbits (2.2-2.7kg) were utilized. Rabbits were purchased from

Sankyo Labo Company, Tokyo. This study was performed according to The Guidelines for the

Treatment of Experimental Animals in Tokyo Dental College. All animals were allowed food

and water ad libitum until the morning of the experiment. The animals were randomly

allocated in two groups: Lidocaine group (n=8) and Saline group (n=8).

Anesthesia was induced by inhalation of 4.0% isoflurane in oxygen delivered using

a mask. Before skin incisions for each of the experimental procedures, appropriate doses of

lidocaine were injected into the surgical field. A #20 Fr non-cuffed pediatric tracheal tube was

inserted into the trachea through tracheostomy. The left auricular marginal vein and right

femoral artery were cannulated with 22- and 20-gauge Teflon indwelling catheters,

respectively. After intravenous acetated Ringer’s solution was started at 10 ml/kg/hr, the

animals were paralyzed with 14 mcg/kg/min rocuronium bromide (Eslax, Schering-Plough,

Tokyo) and mechanically ventilated. End-tidal partial pressure of carbon dioxide (ETCO2) was

maintained at about 35mmHg. Femoral artery blood pressure was continuously monitored with

a pressure transducer (P231D; Gould, Oxnard, California). Heart rate (HR) was recorded by a

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flowmeter (T108; Transonic, Ithaca NY). A flow probe (type 3SB) was applied to the isolated

left common carotid artery. TMBF was measured with a laser Doppler flowmeter (ALF21;

Unique Medical, Tokyo). A contact-type probe (type C; Unique Medical) for TMBF

measurement was placed at the anterior third of the left dorsal surface of the tongue. Care was

taken to minimize the contact pressure of the probe to prevent blood flow disturbance in the

tongue mucosa. Systolic blood pressure (SBP), diastolic blood pressure (DBP), mean arterial

pressure (MAP), HR, CCBF and TMBF were continuously recorded on a polygraph

(Series360 NEC; Sanei, Tokyo).

After the skin incision along both left and right lower margins of the mandible

without local anesthesia, the periosteum of the mandibular body was exposed. The periosteum

was detached to expose the surface of the mandibular body on both side. Two small holes

(approximately 1 mm in diameter, one in the left side and the other in the right side)

perforating into the bone marrow through the cortical bone were drilled with a round bar (ISO.

008, Morita, Japan). Needle probes of a hydrogen clearance tissue blood flowmeter (UHE-100,

Unique Medical, Japan) were inserted 3mm deep into the left and right bone marrow to

measure both left BBF (L-BBF) and right BBF (R-BBF), respectively. In addition, the fascia of

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probes of the hydrogen clearance tissue blood flowmeter were inserted 3mm deep into the left

and right masseter muscle to measure left MBF (L-MBF) and right MBF (R-MBF),

respectively. Then, after the skin incision along the left femoral region without local anesthesia,

the quadriceps muscle was exposed. A needle probe of the hydrogen clearance tissue blood

flowmeter was inserted 5mm deep into the center of the left quadriceps muscle to measure

QBF. Furthermore, after midline laparotomy, two needle probes of the hydrogen clearance

tissue blood flowmeter were inserted 5mm and 2mm deep into the right lobe of the liver just

below xiphoid process of the sternum and the left renal cortex to measure LBF and RBF,

respectively.

After completion of experimental preparations, isoflurane inhalation was

discontinued. Then, inhalation of sevoflurane was started at 1.8% of end-tidal concentration

and maintained at that level for more than 60 min to stabilize the hemodynamic and respiratory

parameters. Sevoflurane concentration was continuously monitored with an anesthetic gas

monitor (Capnmac; Datex, Helsinki). Body temperature was continuously monitored with a

rectal probe and maintained between 39.0 and 39.5℃ with the aid of a heating lamp.

For SGB, the tip of the needle was placed on the left transverse process of the

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ml disposable syringe was used.8 After confirming contact of the tip of the needle with the left

transverse process, either 0.2 ml of 1 % lidocaine (Lidocaine group) or 0.2 ml of normal saline

solution (Saline group) was injected. In Lidocaine group, data were recorded immediately

before SGB (Pre) and at the time when the maximal change in CCBF was observed after SGB

(Post). In Saline group, data were recorded immediately before SGB (Pre) and 3 minutes after

SGB (Post).

In this study, data were expressed as the mean ± standard deviation. The paired t-test

was used for within-group comparisons and the unpaired t-test for between-group comparisons.

P values less than 0.05 were considered statistically significant. All blood flow data in

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Results

Time for the maximal effect was 2.6 ± 0.2 min in Lidocaine group. There were no

differences in respective Pre values between two groups. In Saline group, there were no

differences between Pre and Post values for all observed variables. In contrast, in Lidocaine

group, significant changes from Pre to Post values were observed in CCBF, TMBF, BBF, MBF,

QBF, LBF and RBF. In addition, there were significant differences in respective Post values

between two groups. (Table 1)

In Lidocaine group, Post values for CCBF, TMBF, L-BBF and L-MBF were

significantly increased by 138%, 75%, 60% and 40% in comparison with Pre values,

respectively. In contrast, Post values for R-BBF, R-MBF, QBF, LBF and RBF were

significantly decreased by 40%, 38%, 34%, 9% and 13% in comparison with Pre values,

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Discussion

This study showed that CCBF, TMBF, L-BBF and L-MBF were increased whereas R-BBF,

R-MBF, QBF, LBF and RBF were decreased in Lidocaine group after SGB.

Stellate ganglion was confirmed by exposing cervical sympathetic nerve trunk in our

preliminary study. When SGB was performed based on these results, CCBF was increased

immediately after SGB in a reproducible manner. Consequently, SGB was performed by the

technique written in the method session in this study.

In a previous study, minimum alveolar concentration (MAC) of sevoflurane is 1.5 to

1.8 times as high as that of isoflurane. 9 Therefore, isoflurane was used for induction of

anesthesia and experimental preparations in this study because isoflurane was able to induce

anesthesia more smoothly than sevoflurane. Anesthesia was maintained with 1.8% sevoflurane

throughout experiment. This concentration was equal to almost 0.5 MAC of sevoflurane in the

rabbit.9-12 Sevoflurane has less sympatholytic effects than isofluraneand these effects occur at

the level higher than 0.75 MAC of sevoflurane. 13 Therefore, sevoflurane might minimally

modify the sympatholytic effects of SGB.

In our pilot study, infusion rate of rocuronium bromide which provided stable

(14)

based on a previous study8 and the results of our pilot study, Post values in Saline group were

recorded 3 minutes after SGB. This was almost equal to the time for the maximal change in

CCBF in Lidocaine group. Blood flow in the internal carotid artery (ICA) was increased after

SGB with 2% lidocaine.14 In cases of facial palsy, CCBF and blood flow of the facial nerve

were increased after SGB with 1% mepivacaine.15 CCBF and TMBF were significantly

increased after SGB with 1% lidocaine.8 Based on these reports, it is suggested that the

significant increase in CCBF in this study was caused by the effect of SGB.

An increase in CCBF is dependent on an increase in cardiac output (CO). Increase in CO

is supplied by an afterload (total peripheral resistance) reduction and increases in HR, cardiac

contractility and/or preload (venous return). In this study, no change in HR was observed. In

addition, cardiac contractility and venous return should not increase after SGB because of its

sympatholytic effect. Therefore, it is suggested that significant increase in CCBF was

attributable to CO increase through afterload reduction (vasodilatation). Although afterload

decrease may induce hypotension, blood pressure was unchanged after SGB in this study.

Tissue blood flow in the block side was increased because peripheral vascular resistance at head,

neck and upper limb was decreased after SGB. In contrast, it was speculated that peripheral

(15)

and lower limb were decreased. Therefore, total peripheral resistance might minimally change

in this study. As a result, blood pressure should be unchanged throughout the experiment. This

means that afterload decrease observed in this study was a regional phenomenon based on the

effect of SGB.

Although changes in CCBF result from changes in the blood flow in both ICA and

external carotid artery (ECA), ICA blood flow under normal condition should minimally

change because of the autoregulatory mechanisms of cerebral blood flow. In contrast, ECA

blood flow may change depending on the degree of activations of alpha- and beta-adrenergic

receptors, which innervate blood vessels of skin and mucosa (alpha-adrenergic receptors

dominant) and skeletal muscles (beta-adrenergic receptors dominant).16 Bone marrow blood

flow may change depending on blood pressure. It is suggested that the increases in BBF, MBF

and TMBF on the block side in Lidocaine group resulted from afterload reduction caused by

the sympatholytic effects of SGB. In this study, TMBF and L-MBF were significantly

increased by 75% and 40% in comparison with respective Pre values in Lidocaine group.

Since alpha-adrenergic receptors dominantly exist in the vasculature in head and neck area16, it

may be reasonable that the increase in TMBF was more than that in L-MBF in this study.

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redistribution of that on the non-block side.4,5 However, in this study, QBF, LBF and RBF,

which are out of the sympatholytic effects of SGB, as well as R-BBF and R-MBF on the

non-block side were decreased. Therefore, it is suggested that the increase in blood flow on the

block side is redistributed from not only the non-block side but also lower limb and viscera.

The blood flow of quadriceps muscle, well-vascularized liver and renal cortex17 were adopted

as indicators that were not affected by the sympatholytic effects of SGB in this study.

Quadriceps muscle can be a good indicator for the blood flow of muscular tissue like the

masseter muscle. Similarly, liver and renal cortex can be good indicators for the blood flow of

visceral organ. Biceps brachii muscle blood flow was decreased by 40% whereas liver and

renal blood flow were decreased by 25% to 30% during deliberate hypotention with

trinitroglycerine.18 Hindlimb blood flow was decreased by 60% whereas cerebral blood flow

remained unchanged during deliberate hypotention with sodium nitroprusside.19 When the

circulating blood volume is constant, there is a fundamental mechanism to control tissue blood

flow in vital and non-vital organs as needed through the change of the vascular bed. 20

However, the mechanism of blood flow redistribution is still unclear and to be investigated in

future. Therefore, it is suggested that peripheral tissue blood flow decreased in a compensatory

(17)

were less decreased in comparison with peripheral MBF, TMBF and QBF in this study. Renal

blood flow was decreased by 40% during deliberate hypotention whereas this decrease never

reached the critical level.21 Additionally, there are no reports of impaired liver function during

deliberate hytotention in patients with nomal liver function. 22 In this study, changes in visceral

blood flow after SGB might be of no clinical significance because the decrease in LBF and

RBF were slight and blood pressure showed no major change. Based on the previous studies

and the results of this study, it is suggested that blood flow in peripheral tissue such as lower

limb has more important role on the increase in tissue blood flow after SGB in comparison

with visceral blood flow.

In clinical situations, palm skin temperature at the block side was elevated while that

at the non-block side was lowered following upper thoracic sympathetic ganglion block. 23 In

addition, when lumbar sympathetic ganglion block was performed to the patients with

arteriosclerosis obliterans of lower limbs, blood flow on the non-block side was decreased.24

Therefore, it is suggested that blood flow redistribution to the block side from the non-block

side and the other parts of the body after unilateral sympathetic ganglion block might cause

“steal” phenomenon. Attention should be paid to patients undergoing SGB who have bilateral

(18)

There are some reports focusing on the effect of SGB on coronary hemodynamics.

It is reported that SGB has deteriorative effects on the myocardial oxygen supply-demand

relationship with normal coronary circulation in the dog. 25 In that study, coronary artery blood

flow was measured whereas myocardial oxygen consumption and oxygen extraction ratio were

calculated. In addition, myocardial blood flow and tissue oxygen tension were not measured.25

Therefore, the effect of SGB on coronary hemodynamics still remains controversial and is to

be investigated.

In conclusion, it is suggested that lower limb and visceral blood flow as well as the

non-block side are redistributed to the block side after SGB. Peripheral tissue blood flow has

(19)

References

1) Barash PG, Cullen BF, Stoelting RK. Peripheral nerve blockade. In: Mulroy MF. Clinical

Anesthesia. 2nd ed, Philadelphia, PA: Lippincott, 1992.

2) Milligan NS, Nash TP: Treatment of post-herpetic neuralgia. A review of 77 consecutive

cases. Pain 1985; 23: 381-386.

3) Salvaggio I, Adducci E, Dell’vAquila L et al: Facial pain: a possible therapy with stellate

ganglion block. Pain Med 2008; 9: 958-962.

4) Yamazaki Y, Mimura T, Iwasaki F, Namiki A: Regional cerebral blood flow and

oxygenation following cervicothoracic sympathetic block. Masui 1998; 47: 1233-1236.

5) Okuda Y, Kitajima T: Influence of stellate ganglion block on bilateral cervicobrachial

arterial and venous blood flow. Masui 1994; 43: 1201-1206.

6) Kakuyama M, Toda H, Osawa M, Fukuda K. The bilateral effect on stellate ganglion block

on the facial skin blood flow. Reg Anesth Pain Med 2000; 25: 389-392.

7) Mineta M, Takeda Y, Matoba M et al: Change of the blood flow in celiac artery and superior

mesenteric artery after stellate ganglion block. Masui 1993; 42: 1808-1812.

8) Terakawa Y, Handa M, Ichinohe T, Kaneko Y: Epinephrine in local anesthetic cancels

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Coll 2007; 48: 37-42.

9) Scheller MS, Saidman LJ, Brian L: MAC of sevoflurane in humans and the New Zealand

White rabbit. Can J Anaesh 1988; 35: 153-156.

10) Ichinohe T, Homma Y, Kaneko Y: Mucosal blood flow during various intravenous and

inhalational anesthetics in the rabbit. Oral Surg Oral Med Oral Pathol Oral Radiol Endod

1998; 85: 268-271.

11) Kemmochi M, Ichinohe T, Kaneko Y: Remifentanil decreases mandibular bone marrow

blood flow during propofol and sevoflurane anesthesia in rabbits. J Oral Maxillofac Surg

2009; in press.

12) Handa M, Ichinohe T, Kaneko Y: Changes in partial pressure of arterial carbon dioxide

induces redistribution oral tissue blood flow in the rabbit. J Oral Maxillofac Surg 2008; 66:

1820-1825.

13) Akata T, Kobama K, Takahashi S: Volatile anesthetic action on norepinephrine-induced

contraction of small splanchnic resistance arteries. Can J Anesth 1995; 42: 1040-1050.

14) Liu F, Xu G, Liu Z, Zhao Y, Lv X, Wang J: The effects of stellate ganglion block on visual

evoked potential and blood flow of the ophthalmic and internal carotid arteries in patients with

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15) Murakawa K: Changes in microcirculation in the facial nerve with electrical stimulation

and chemical blockade of cervical sympathetic trunks. Masui 1993; 42: 646-652.

16) Thomas CW, David PW. Neurotransmission. In: Westfall TC, Westfall DP. Goodman &

Gilman’s The Pharmacological Basis of Therapeutics. 11th ed. New York, NY: Lippincott

Brunton LL, Lazo JS, Parker KL, 2006.

17) Brezis M, Rosen S. Hypoxia of the renal medulla -its implications for disease. N Engl J

Med 1995; 332: 647-655.

18) Kobori M, Negishi H, Hosoyamada A. Influence of hypotensive anesthesia on the organ

blood flow –Comparison of trinitoroglycerine and nicardipine-. Masui 1995; 44: 956-962.

19) Chang CL, Yeh FC, Ho W, Chen HI. Effects of sodium nitropurusside-induced hypotention

on the cerebral and hindlimb blood flow in dogs. Proc Natl Sci Counc Repub China B 1985; 9:

202-207.

20) DeBakey ME, Burch G, Ray T et al: The borrowing- lending hemodynamic phenomenon

(Hemometakinesia) and its therapeutic application in peripheral vascular disturbances. Ann

Surg 1947; 126:850-865.

21) Kick O, Aken HV, Wouters PF, Verbesselt K, Hemelrijck JV. Vital organ blood flow during

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22) Rodrigo C. Induced hypotention during anesthesia, with special reference to orthognathic

surgery. Anesth Prog 1995; 42: 41-58.

23) Hashizume K, Yamagami A, Yoshikawa M, Furuya J. Clinical evaluation of “borrowing-

lending” phenomenon in the upper limbs following upper thoracic sympathetic ganglion block.

Pain Clinic 1996; 17: 389-392. (In Japanese)

24) Baron HC, Hiesiger E, Sabri M. Undesirable effects of hemometakinesia induced vascular

reconstruction. Surg Gynecol Obstet 1979; 148: 534-538.

25) Sasaki I, Kaneko T, Iwatsuki N, Hashimoto Y. Effects of stellate ganglion block on

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Tables

Table 1 Hemodynamic variables and blood flow data

Saline group Lidocaine group

Pre Post Pre Post

HR (bpm) 268.1±17.7 265.9±17.1 269.0±19.2 270.6±20.8 SBP (mmHg) 119.9±11.7 121.8±10.9 124.3±6.4 123.7±7.5 DBP (mmHg) 63.8±10.3 64.4±10.2 54.6±5.5 55.0±7.1 MAP (mmHg) 81.3±12.2 80.6±12.9 78.5±6.5 79.8±5.4 CCBF (ml/min) 21.8±5.5 21.1±5.7 20.2±4.0 48.0±17.6*# TMBF (ml/min/100g) 23.6±4.4 22.9±3.9 20.2±1.3 35.2±4.5*# L-BBF (ml/min/100g) 41.3±5.2 44.0±7.8 43.9±12.7 70.5±26.1*# R-BBF (ml/min/100g) 48.0±9.2 49.9±11.5 45.2±9.0 27.3±6.5*# L-MBF (ml/min/100g) 48.9±6.8 47.3±7.0 49.6±10.6 69.6±13.5*# R-MBF (ml/min/100g) 47.3±8.6 48.3±9.0 55.2±11.6 34.3±8.3*# QBF (ml/min/100g) 60.6±14.8 63.7±11.2 57.9±18.0 38.2±12.8*# LBF (ml/min/100g) 80.9±10.7 83.7±8.7 76.3±13.6 69.4±14.4*# RBF (ml/min/100g) 167.6±19.6 168.7±18.8 159.7±27.6 138.8±23.5*#

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HR: heart rate; SBP: systolic blood pressure; DBP: diastolic blood pressure; MAP: mean

arterial pressure; CCBF: common carotid artery blood flow; TMBF: tongue mucosal blood

flow; BBF: mandibular bone marrow blood flow; MBF: masseter muscle blood flow; QBF:

quadriceps muscle blood flow; LBF: liver blood flow; RBF: renal blood flow

L: left side; R: right side

Pre: immediately before SGB

Post: at the time when maximal change in CCBF was observed after SGB (Lidocaine group) or

3 minutes after SGB (Saline group)

mean ± standard deviation (n=8)

*p<0.05 vs Pre

#

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Legends for figures

Fig. 1 Changes in tissue blood flow in the Lidocaine group.

Data were expressed as the percentage of respective Pre value in the Lidocaine group.

CCBF: common carotid artery blood flow; TMBF: tongue mucosal blood flow; BBF:

mandibular bone marrow blood flow; MBF: masseter muscle blood flow; QBF: quadriceps

muscle blood flow; LBF: liver blood flow; RBF: renal blood flow

L: left side; R: right side

Pre: immediately before SGB

Post: at the time when maximal change in CCBF was observed after SGB (Lidocaine group) or

3 minutes after SGB (Saline group)

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Table 1  Hemodynamic variables and blood flow data

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